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目的 :研究非钙依赖性的磷脂酶A2 (PLA2 )和ATP敏感性钾通道 (KATP)在大鼠心肌缺血再灌注(I/R)心律失常中的作用。方法 :结扎大鼠左冠状动脉前降支造成缺血 10min ,然后放开再灌注 10min。在心肌缺血前 5min分别给予PLA2 抑制剂 5 ,5 -dithio -bis(2 -nitrobenzoicacid) (DTNB) (16mg/kg) ,KATP开放剂pinacidil(0 2mg/kg) ,KATP阻断剂glibenclamide(0 3mg/kg)。结果 :与对照组相比 ,DTNB可降低心律失常评分、磷酸肌酸激酶 (CPK)和乳酸脱氢酶 (LDH)值 (P <0 0 5 ) ;而glibenclamide对I/R心律失常无影响 ,但升高CPK ,LDH值 (P<0 0 5 ) ;与glibenclamide组比 ,在glibenclamide阻断KATP后 ,DTNB可引起致死性心律失常 ,并可升高LDH值 (P<0 0 5 ) ;pinacidil可完全抑制I/R引起的室颤和室速。结论 :PLA2 抑制剂DTNB可减轻I/R损伤 ,表明PLA2 在I/R心律失常中起着重要作用 ,同时也表明激活的KATP具有抗I/R心律失常的作用。但DTNB对抗I/R心律失常的作用与KATP的关系仍有待进一步研究。
AIM: To investigate the role of non-calcium-dependent phospholipase A2 (PLA2) and ATP-sensitive potassium channels (KATP) in arrhythmia of myocardial ischemia-reperfusion (I / R) in rats. Methods: Ligation of left anterior descending coronary artery caused ischemia 10min, and then let go 10min reperfusion. PLA2 inhibitor 5, 5-dithio-bis (DTNB) (16 mg / kg), KATP opener pinacidil (0 2 mg / kg) and KATP blocker glibenclamide 3 mg / kg). Results: Compared with the control group, DTNB reduced arrhythmia score, creatine phosphokinase (CK) and lactate dehydrogenase (LDH) values (P <0 05), while glibenclamide had no effect on I / R arrhythmia, (P <0 05). Compared with glibenclamide group, DTNB could induce fatal arrhythmia and increase LDH (P <0 05) after glibenclamide blocked KATP; and pinacidil Can completely inhibit I / R-induced ventricular fibrillation and ventricular tachycardia. CONCLUSION: PLA2 inhibitor DTNB can reduce I / R injury, indicating that PLA2 plays an important role in I / R cardiac arrhythmia. It also shows that activated KATP has anti-I / R arrhythmia. However, the role of DTNB against I / R arrhythmia and its relationship with KATP remains to be further studied.